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本实验在大鼠小肠缺血再灌注（I/R）损伤模型上观察左族精氨酸（L－Arginine，L-Arg）和左旋硝基精氨酸（L－NNA）对缺血预处理（IPC）和I／R损伤的影响，旨在探讨内皮源性舒张因子/1-氧化氮(endothlium-derivedrelaxingfactor/nitricoxide,EDRF/ND）系统在IPC细胞保护中的作用。结果表明IPC能减轻小肠I/R后血压下降程度（8．3±2．5vs5．6±0．9kPa，P＜0．01），及肠粘膜出血，减少LDH漏出（0．6±0．4vs1．1±0．4U／L），MDA产生（112．9±3．7vs370．1±27.5mmol/g）；明显改善肠道血管床功能，使伊文思兰渗出减少（153．8±36．6vs341．1±429μg/g，P＜0．01），MPO活性下降（24．6±12．8vs79．9±11．5U/g，P＜0．01）。LPC还使血浆NO2含量升高（3．2±1．0vs1．0±0．2μmol/L，P＜0．01），ET水平下降。L－NNA完全消除IP的保护作用，L-Arg则模拟了IPC的保护作用。提示：IPC对I/R损伤小肠有保护作用，EDRF／NO系统的激活参与了这种保护。
In this study, L-Arginine (L-Arginine) and L-NNA (L-Arginine) on ischemia / reperfusion (I / R) (IPC) and I / R injury in order to explore the role of endothlium-derived protective factor / nitric oxide (EDRF / ND) system in IPC cytoprotection. The results showed that IPC could relieve the decrease of blood pressure after I / R in small intestine (8.3 ± 2.5 vs 5.6 ± 0.9kPa, P <0.01), and intestinal mucosal hemorrhage and decrease LDH leakage (0.6 ± 0. 4vs1.1 ± 0.4U / L) and MDA production (112.9 ± 3.7vs370.1 ± 27.5mmol / g), significantly improved the function of intestinal vascular bed and reduced the evacuation of Evans blue (153.8 ± 36.6vs341.1 ± 429μg / g, P <0.01), MPO activity decreased (24.6 ± 12.8vs79.9 ± 11.5U / g, P <0.01). LPC also increased plasma NO2 level (3.2 ± 1.0vs1.0 ± 0.2μmol / L, P <0.01), ET levels decreased. L-NNA completely eliminates the protective effects of IP, whereas L-Arg mimics the protective effect of IPC. Tip: IPC has protective effect on I / R injured small intestine, and activation of EDRF / NO system is involved in this protection.